Preeclampsia is characterized by the development of hypertension and kidney dysfunction during late stages of pregnancy, and it is an important cause of maternal and fetal mortality. Quitterer et al. found that increased complex formation between the G protein–coupled receptors angiotensin II AT1 and bradykinin B2 in vascular smooth muscle cells triggered preeclampsia in pregnant mice. Evidence for the hyperactivity of this heterodimer was also found in vascular structures in samples of placenta from pregnancies that had preeclampsia. Using a small-molecule inhibitor to target AT1-B2 receptor signaling prevented preeclampsia in mice. Initial data in patients with symptoms of preeclampsia indicate that this is an avenue for treatment options.